Disease resistance genes are defined as Mendelian factors that cosegregate with the resistance trait. The gene HM1, which controls resistance to Cochliobolus carbonum Nelson race 1 was among the first disease resistance genes to be described. The disease caused by C. carbonum race 1 can be devastating, resulting in yield losses of 80% or more due to plant death and grain mold. The dominant allele, Hm1, and the duplicate factor, Hm2 are the only disease resistance genes that are known to be fixed at a high frequency in maize germplasm.
Since the discovery of a race-specific compatibility factor that is produced by the fungus, the disease caused by C. carbonum race 1 has been the subject of detailed study. This compatibility factor permits the fungus to infect certain genotypes of maize that would otherwise be resistant. The role of HM1 in providing resistance to the fungus is a function of its ability to cause reduced sensitivity to the compatibility factor. Further studies established that the presence of the compatibility factor confers the same race-specificity (for hm1/hm1 corn) on the oat pathogen, Cochliobolus victoriae. The structure of this compatibility factor, HC-toxin, is known but the mode of action remains to be elucidated. Recently, an enzyme that inactivates HC-toxin has been identified in extracts from maize. The enzyme, HC-toxin reductase (HCTR), is detectable only in extracts from resistant (Hm1) genotypes. This establishes HCTR activity as the biochemical phenotype of Hm1.